| Angiotensin receptor blockers: evidence for preserving target organs. | |
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MedLine Citation:
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PMID: 11288962 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Hypertension is a major problem throughout the developed world. Although current antihypertensive treatment regimens reduce morbidity and mortality, patients are often noncompliant, and medications may not completely normalize blood pressure. As a result, current therapy frequently does not prevent or reverse the cardiovascular remodeling that often occurs when blood pressure is chronically elevated. Blockade of the renin-angiotensin system (RAS) is effective in controlling hypertension and treating congestive heart failure. Both angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) inhibit the activity of the RAS, but these two classes of antihypertensive medications have different mechanisms of action and different pharmacologic profiles. Angiotensin-converting enzyme inhibitors block a single pathway in the production of angiotensin II (Ang II). In addition, angiotensin I is not the only substrate for ACE. The ACE inhibitors also block the degradation of bradykinin that may have potential benefits in cardiovascular disease. Bradykinin is, however, the presumed cause of cough associated with ACE inhibitor therapy. Data from clinical trials on ACE inhibitors serve to support the involvement of the RAS in the development of cardiovascular disease. Angiotensin receptor blockers act distally in the RAS to block the Ang II type 1 (AT1) receptor selectively. Thus, ARBs are more specific agents and avoid many side effects. Experimental and clinical trials have documented the efficacy of ARBs in preserving target-organ function and reversing cardiovascular remodeling. In some instances, maximal benefit may be obtained with Ang II blockade using both ARBs and ACE inhibitors. This review describes clinical trials that document the efficacy of ARBs in protecting the myocardium, blood vessels, and renal vasculature. |
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Authors:
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P Carson; T Giles; M Higginbotham; N Hollenberg; W Kannel; H M Siragy |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Clinical cardiology Volume: 24 ISSN: 0160-9289 ISO Abbreviation: Clin Cardiol Publication Date: 2001 Mar |
Date Detail:
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Created Date: 2001-04-05 Completed Date: 2001-07-26 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 7903272 Medline TA: Clin Cardiol Country: United States |
Other Details:
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Languages: eng Pagination: 183-90 Citation Subset: IM |
Affiliation:
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Department of Cardiology, Veterans Affairs Medical Center, Washington, DC, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin-Converting Enzyme Inhibitors
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pharmacology,
therapeutic use Antihypertensive Agents / pharmacology, therapeutic use Chronic Disease Drug Therapy, Combination Heart Failure / drug therapy, physiopathology Hemodynamics Humans Hypertension / drug therapy*, physiopathology* Hypertrophy, Left Ventricular / drug therapy, physiopathology Myocardial Infarction / drug therapy, physiopathology Receptors, Angiotensin / antagonists & inhibitors* Renin-Angiotensin System / drug effects, physiology |
| Chemical | |
Reg. No./Substance:
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0/Angiotensin-Converting Enzyme Inhibitors; 0/Antihypertensive Agents; 0/Receptors, Angiotensin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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